Acidosis slows electrical conduction through the atrio-ventricular node.

Ashley M Nisbet,Nicola L Walker,Godfrey L Smith,Clive H Orchard,Margaret A Craig,Hongwei Cheng,Francis L Burton,Jules C Hancox

doi:10.3389/fphys.2014.00233

Ashley M Nisbet, Nicola L Walker + Show 6 more

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https://doi.org/10.3389/fphys.2014.00233

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Abstract

Acidosis affects the mechanical and electrical activity of mammalian hearts but comparatively little is known about its effects on the function of the atrio-ventricular node (AVN). In this study, the electrical activity of the epicardial surface of the left ventricle of isolated Langendorff-perfused rabbit hearts was examined using optical methods. Perfusion with hypercapnic Tyrode's solution (20% CO2, pH 6.7) increased the time of earliest activation (Tact) from 100.5 ± 7.9 to 166.1 ± 7.2 ms (n = 8) at a pacing cycle length (PCL) of 300 ms (37°C). Tact increased at shorter PCL, and the hypercapnic solution prolonged Tact further: at 150 ms PCL, Tact was prolonged from 131.0 ± 5.2 to 174.9 ± 16.3 ms. 2:1 AVN block was common at shorter cycle lengths. Atrial and ventricular conduction times were not significantly affected by the hypercapnic solution suggesting that the increased delay originated in the AVN. Isolated right atrial preparations were superfused with Tyrode's solutions at pH 7.4 (control), 6.8 and 6.3. Low pH prolonged the atrial-Hisian (AH) interval, the AVN effective and functional refractory periods and Wenckebach cycle length significantly. Complete AVN block occurred in 6 out of 9 preparations. Optical imaging of conduction at the AV junction revealed increased conduction delay in the region of the AVN, with less marked effects in atrial and ventricular tissue. Thus acidosis can dramatically prolong the AVN delay, and in combination with short cycle lengths, this can cause partial or complete AVN block and is therefore implicated in the development of brady-arrhythmias in conditions of local or systemic acidosis.

Highlights

Slow electrical conduction through the atrio-ventricular node (AVN) normally ensures correct timing of atrial and ventricular contraction (Meijler and Janse, 1988)
The time to earliest epicardial activation was prolonged at each pacing cycle length (PCL), with the effect becoming more pronounced at shorter PCL
EFFECTS OF ACIDOSIS ON THE AV JUNCTION The present study provides the first direct evidence that acidosis significantly alters the function of the AVN, slowing conduction and prolonging the refractory period, manifested in the whole heart as slowed AV conduction and, at short PCL and low pH, complete AV conduction block

Summary

Introduction

Slow electrical conduction through the AVN normally ensures correct timing of atrial and ventricular contraction (Meijler and Janse, 1988). The critical roles of the AVN in normal and aberrant electrical conduction make it a region of major clinical importance. Pathological conditions such as myocardial ischemia and systemic acidosis result in exposure of the heart to acidic conditions (Elliott et al, 1992). Purkinje fiber excitability is altered by exposure to low pH (Brown et al, 1978), whilst the spontaneous rate of sinoatrial nodal cell and small tissue preparations shows marked pH sensitivity (Satoh and Hashimoto, 1983; Satoh and Seyama, 1986).Work on the intact rat heart implicates the AVN as a major cardiac site of action of acidosis (Aberra et al, 2001); electrocardiogram measurements have shown both heart rate reduction and propranolol- and atropine-insensitive prolongation of the PR interval with acidosis (Aberra et al, 2001), unaccompanied by significant changes to the QRS complex. Non-compensated lactic acidosis associated with salicylic acid (aspirin) poisoning has been associated with third degree AV block, whilst toxic adenoma of the thyroid gland has been associated, albeit rarely, with complete heart block accompanied by metabolic acidosis (Pena-Alonso et al, 2003)

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